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Ernesto Alfaro-Moreno,¹ Leticia Martínez,² Claudia García-Cuellar,¹ James C. Bonner,³ J. Clifford Murray,⁴ Irma Rosas,² Sergio Ponce de León Rosales,⁵ and Álvaro R. Osornio-Vargas¹

¹Instituto Nacional de Cancerología, Mexico D.F., Mexico; ²Centro de Ciencias de la Atmósfera, Universidad Nacional Autónama de Mexico, Mexico D.F., Mexico; ³National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA; ⁴University of Nottingham, Nottingham, United Kingdom; ⁵Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán," Mexico D.F., Mexico

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 (TNF) , interleukin 6 (IL-6) , prostaglandin E₂ (PGE₂) ] (enzyme-linked immunosorbent assay) , and E-selectin (flow cytometry) in cell lines exposed to particulate matter < 10 µm in size (PM₁₀) obtained from the northern, central, and southern zones of Mexico City. Particle concentrations ranged from 2.5 to 160 µg/cm². We used epithelial, endothelial, fibroblastic, and monocytic cells and assessed DNA damage in Balb-c cells, TNF 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. Key words: apoptosis, cytotoxicity, DNA breakage, E-selectin, IL-6, Mexico City, particle composition, PGE₂, PM₁₀, TNF. Environ Health Perspect 110:715-720 (2002) . [Online 4 June 2002]

http://ehpnet1.niehs.nih.gov/docs/2002/110p715-720alfaro-moreno/ abstract.html

Address correspondence to Á.R.Osornio-Vargas, Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando 22, Tlalpan, México, D.F., 14000. Telephone: (5255) 5628-0425. Fax: (5255) 5628-0432. E-mail: arov@servidor.unam.mx

We thank A. Rice, W. Ward, and E. Salinas for technical support, K. Dreher (U.S. Environmental Protection Agency) and R. Ramos (Red Automática de Monitoreo Ambiental, Gobierno del Distrito Federal) for providing PM₁₀ analysis and air pollution data, respectively.

This research was partially supported by CONSERVA-1999, CONACYT (F-383-M9304 ; 87862, 34547-M) , DGEP-UNAM, and the Academia Mexicana de Ciencias-Royal Society.

Received 6 July 2001 ; accepted 17 December 2001.