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Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe.
Inhal Toxicol. 2008 Nov; 20(14):1215-31.IT

Abstract

Inflammation is regarded as an important mechanism in mortality and morbidity associated with exposures of cardiorespiratory patients to urban air particulate matter. We investigated the association of the chemical composition and sources of urban air fine (PM(2.5-0.2)) and coarse (PM(10-2.5)) particulate samples with the inflammatory activity in the mouse lung. The particulate samples were collected during selected seasons in six European cities using a high-volume cascade impactor. Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. At 4, 12, and 24 h after the exposure, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cell number, total protein, and cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, and KC). Dicarboxylic acids and transition metals, especially Ni and V, in PM(2.5-0.2) correlated positively and some secondary inorganic ions (NO3(-), NH4(+)) negatively with the inflammatory activity. Total organic matter and SO4(2-) had no consistent correlations. In addition, the soil-derived constituents (Ca2+, Al, Fe, Si) showed positive correlations with the PM(2.5-0.2)-induced inflammatory activity, but their role in PM(10-2.5) remained obscure, possibly due to largely undefined biogenic material. Markers of poor biomass and coal combustion, i.e., monosaccharide anhydrides and As, were associated with elevated PAH contents in PM(2.5-0.2) and a consistent immunosuppressive effect. Overall, our results support epidemiological findings that the local sources of incomplete combustion and resuspended road dust are important in urban air particulate pollution-related health effects.

Authors+Show Affiliations

National Public Health Institute and University of Kuopio, Kuopio, Finland. Mikko.Happo@ktl.fiNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18855153

Citation

Happo, Mikko S., et al. "Chemical Compositions Responsible for Inflammation and Tissue Damage in the Mouse Lung By Coarse and Fine Particulate Samples From Contrasting Air Pollution in Europe." Inhalation Toxicology, vol. 20, no. 14, 2008, pp. 1215-31.
Happo MS, Hirvonen MR, Halinen AI, et al. Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe. Inhal Toxicol. 2008;20(14):1215-31.
Happo, M. S., Hirvonen, M. R., Halinen, A. I., Jalava, P. I., Pennanen, A. S., Sillanpaa, M., Hillamo, R., & Salonen, R. O. (2008). Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe. Inhalation Toxicology, 20(14), 1215-31. https://doi.org/10.1080/08958370802147282
Happo MS, et al. Chemical Compositions Responsible for Inflammation and Tissue Damage in the Mouse Lung By Coarse and Fine Particulate Samples From Contrasting Air Pollution in Europe. Inhal Toxicol. 2008;20(14):1215-31. PubMed PMID: 18855153.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chemical compositions responsible for inflammation and tissue damage in the mouse lung by coarse and fine particulate samples from contrasting air pollution in Europe. AU - Happo,Mikko S, AU - Hirvonen,Maija-Riitta, AU - Halinen,Arja I, AU - Jalava,Pasi I, AU - Pennanen,Arto S, AU - Sillanpaa,Markus, AU - Hillamo,Risto, AU - Salonen,Raimo O, PY - 2008/10/16/pubmed PY - 2009/1/14/medline PY - 2008/10/16/entrez SP - 1215 EP - 31 JF - Inhalation toxicology JO - Inhal Toxicol VL - 20 IS - 14 N2 - Inflammation is regarded as an important mechanism in mortality and morbidity associated with exposures of cardiorespiratory patients to urban air particulate matter. We investigated the association of the chemical composition and sources of urban air fine (PM(2.5-0.2)) and coarse (PM(10-2.5)) particulate samples with the inflammatory activity in the mouse lung. The particulate samples were collected during selected seasons in six European cities using a high-volume cascade impactor. Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. At 4, 12, and 24 h after the exposure, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cell number, total protein, and cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, and KC). Dicarboxylic acids and transition metals, especially Ni and V, in PM(2.5-0.2) correlated positively and some secondary inorganic ions (NO3(-), NH4(+)) negatively with the inflammatory activity. Total organic matter and SO4(2-) had no consistent correlations. In addition, the soil-derived constituents (Ca2+, Al, Fe, Si) showed positive correlations with the PM(2.5-0.2)-induced inflammatory activity, but their role in PM(10-2.5) remained obscure, possibly due to largely undefined biogenic material. Markers of poor biomass and coal combustion, i.e., monosaccharide anhydrides and As, were associated with elevated PAH contents in PM(2.5-0.2) and a consistent immunosuppressive effect. Overall, our results support epidemiological findings that the local sources of incomplete combustion and resuspended road dust are important in urban air particulate pollution-related health effects. SN - 1091-7691 UR - https://www.unboundmedicine.com/medline/citation/18855153/Chemical_compositions_responsible_for_inflammation_and_tissue_damage_in_the_mouse_lung_by_coarse_and_fine_particulate_samples_from_contrasting_air_pollution_in_Europe_ L2 - https://www.tandfonline.com/doi/full/10.1080/08958370802147282 DB - PRIME DP - Unbound Medicine ER -