Biologic effects induced in vitro by PM10 from three different zones of Mexico City.

Abstract

Exposure to urban airborne particles is associated with an increase in morbidity and mortality. There is little experimental evidence of the mechanisms involved and the role of particle composition. We assessed cytotoxicity (crystal violet assay), apoptosis [terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) or annexin V assay], DNA breakage (comet assay), and production of proinflammatory mediators [tumor necrosis factor Alpha (TNF-Alpha), interleukin 6 (IL-6), prostaglandin E2 (PGE2)] (enzyme-linked immunosorbent assay), and E-selectin (flow cytometry) in cell lines exposed to particulate matter < 10 microm in size (PM10) obtained from the northern, central, and southern zones of Mexico City. Particle concentrations ranged from 2.5 to 160 microg/cm(2). We used epithelial, endothelial, fibroblastic, and monocytic cells and assessed DNA damage in Balb-c cells, TNF-Alpha and IL-6 production in mouse monocytes, and PGE2 in rat lung fibroblasts. We determined the expression of E-selectin in human endothelial cells and evaluated the cytotoxic potential of the PM10 samples in all cell types. PM10 from all three zones of Mexico City caused cell death, DNA breakage, and apoptosis, with particles from the north and central zones being the most toxic. All of these PM10 samples induced secretion of proinflammatory molecules, and particles from the central zone were the most potent. Endothelial cells exposed to PM10 from the three zones expressed similar E-selectin levels. Mexico City PM10 induced biologic effects dependent on the zone of origin, which could be caused by differences in the mixture or size distribution within particle samples. Our data suggest that particle composition as well as particle size should be considered in assessing the adverse effects of airborne particulate pollution.

Cytotoxic response in human lung epithelial cells and ion characteristics of urban-air particles from Torino, a northern Italian city

“…(Frampton et al 1999 ) and contaminants adsorbed on the particles (Baulig et al 2003 ;Billet et al 2007 ;Calcabrini et al 2004 ;Frampton et al 1999 ;Muller et al 2006 ). In this study, PM10 and PM2.5 extracts inhibited cell proliferation and induced LDH release in a dose-dependent manner, similar to the results found in other studies on epithelial cells (Alfaro-Moreno et al 2002 ;Osornio-Vargas et al 2003 ;Schiliroò et al 2010 ). Significant seasonal trends were observed only with the organic PM10 extracts; otherwise, the effects produced by the samples from cold seasons were similar to those induced by the other samples.…”

Nanoparticle-driven DNA damage mimics irradiation-related carcinogenesis pathways

“…The ability of Tbh or BaP to induce DSBs is a topic of ongoing debate. The present data are consistent with findings of DNA breaks in Balb-c cells exposed to PM10 by ALFARO-MORENO et al [42] and BUSCHINI et al [43], who found that NP fraction of airborne particulate generally caused the most DNA damage in human lung fibroblasts. In the present study, exposure of A549 cells to UD resulted in transient arrest of cell cycle passage.…”

Fine and Coarse Particulate Matter Chemical Characterization in a Heavily Industrialized City in Central Mexico during Winter 2003

“…[1][2][3][4][5][6][7][8][9][10][11] The Mexican Health Bureau, Secretaría de Salud, revised the previous National Ambient Air Quality for particles 12 establishing a 24-hr average concentration limit of 65 g m Ϫ3 and an annual average concentration of 15 g m Ϫ3 for PM 2.5 and also modified the PM with aerodynamic diameter of less than 10 m (PM 10 ) 24-hr average concentration limit to 120 g m…”