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. 2003 Aug;111(10):1289–1293. doi: 10.1289/ehp.5913

Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.

Alvaro R Osornio-Vargas 1, James C Bonner 1, Ernesto Alfaro-Moreno 1, Leticia Martínez 1, Claudia García-Cuellar 1, Sergio Ponce-de-León Rosales 1, Javier Miranda 1, Irma Rosas 1
PMCID: PMC1241608  PMID: 12896848

Abstract

Exposure to urban airborne particulate matter (PM) is associated with adverse health effects. We previously reported that the cytotoxic and proinflammatory effects of Mexico City PM10 (less than or equal to 10 micro m mean aerodynamic diameter) are determined by transition metals and endotoxins associated with these particles. However, PM2.5 (less than or equal to 2.5 micro m mean aerodynamic diameter) could be more important as a human health risk because this smaller PM has the potential to reach the distal lung after inhalation. In this study, we compared the cytotoxic and proinflammatory effects of Mexico City PM10 with those of PM2.5 using the murine monocytic J774A.1 cell line in vitro. PMs were collected from the northern zone or the southeastern zone of Mexico City. Elemental composition and bacterial endotoxin on PMs were measured. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) production by J774A.1 cells was measured in the presence or absence of recombinant endotoxin-neutralizing protein (rENP). Both northern and southeastern PMs contained endotoxin and a variety of transition metals. Southeastern PM10 contained the highest endotoxin levels, 2-fold higher than that in northern PM10. Northern and southeastern PM2.5 contained the lowest endotoxin levels. Accordingly, southeastern PM10 was the most potent in causing secretion of the proinflammatory cytokines TNF-alpha and IL-6. All PM2.5 and PM10 samples caused cytotoxicity, but northern PMs were the most toxic. Cytokine secretion induced by southeastern PM10 was reduced 50-75% by rENP. These results indicate major differences in PM10 and PM2.5. PM2.5 induces cytotoxicity in vitro through an endotoxin-independent mechanism that is likely mediated by transition metals. In contrast, PM10 with relatively high levels of endotoxin induces proinflammatory cytokine release via an endotoxin-dependent mechanism.

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Selected References

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  1. Alfaro-Moreno Ernesto, Martínez Leticia, García-Cuellar Claudia, Bonner James C., Murray J. Clifford, Rosas Irma, Rosales Sergio Ponce de León, Osornio-Vargas Alvaro R. Biologic effects induced in vitro by PM10 from three different zones of Mexico City. Environ Health Perspect. 2002 Jul;110(7):715–720. doi: 10.1289/ehp.02110715. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Bonner J. C., Rice A. B., Lindroos P. M., O'Brien P. O., Dreher K. L., Rosas I., Alfaro-Moreno E., Osornio-Vargas A. R. Induction of the lung myofibroblast PDGF receptor system by urban ambient particles from Mexico City. Am J Respir Cell Mol Biol. 1998 Oct;19(4):672–680. doi: 10.1165/ajrcmb.19.4.3176. [DOI] [PubMed] [Google Scholar]
  3. Branch D. R., Shah A., Guilbert L. J. A specific and reliable bioassay for the detection of femtomolar levels of human and murine tumor necrosis factors. J Immunol Methods. 1991 Oct 25;143(2):251–261. doi: 10.1016/0022-1759(91)90050-p. [DOI] [PubMed] [Google Scholar]
  4. Diociaiuti M., Balduzzi M., De Berardis B., Cattani G., Stacchini G., Ziemacki G., Marconi A., Paoletti L. The two PM(2.5) (fine) and PM(2.5-10) (coarse) fractions: evidence of different biological activity. Environ Res. 2001 Jul;86(3):254–262. doi: 10.1006/enrs.2001.4275. [DOI] [PubMed] [Google Scholar]
  5. Dreher K. L., Jaskot R. H., Lehmann J. R., Richards J. H., McGee J. K., Ghio A. J., Costa D. L. Soluble transition metals mediate residual oil fly ash induced acute lung injury. J Toxicol Environ Health. 1997 Feb 21;50(3):285–305. [PubMed] [Google Scholar]
  6. Dye J. A., Lehmann J. R., McGee J. K., Winsett D. W., Ledbetter A. D., Everitt J. I., Ghio A. J., Costa D. L. Acute pulmonary toxicity of particulate matter filter extracts in rats: coherence with epidemiologic studies in Utah Valley residents. Environ Health Perspect. 2001 Jun;109 (Suppl 3):395–403. doi: 10.1289/ehp.01109s3395. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Gorczyca W., Gong J., Ardelt B., Traganos F., Darzynkiewicz Z. The cell cycle related differences in susceptibility of HL-60 cells to apoptosis induced by various antitumor agents. Cancer Res. 1993 Jul 1;53(13):3186–3192. [PubMed] [Google Scholar]
  8. Holian A., Hamilton R. F., Jr, Morandi M. T., Brown S. D., Li L. Urban particle-induced apoptosis and phenotype shifts in human alveolar macrophages. Environ Health Perspect. 1998 Mar;106(3):127–132. doi: 10.1289/ehp.98106127. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Hsiao W. L., Mo Z. Y., Fang M., Shi X. M., Wang F. Cytotoxicity of PM(2.5) and PM(2.5--10) ambient air pollutants assessed by the MTT and the Comet assays. Mutat Res. 2000 Nov 20;471(1-2):45–55. doi: 10.1016/s1383-5718(00)00116-9. [DOI] [PubMed] [Google Scholar]
  10. Kueng W., Silber E., Eppenberger U. Quantification of cells cultured on 96-well plates. Anal Biochem. 1989 Oct;182(1):16–19. doi: 10.1016/0003-2697(89)90710-0. [DOI] [PubMed] [Google Scholar]
  11. Levy J. I., Hammitt J. K., Spengler J. D. Estimating the mortality impacts of particulate matter: what can be learned from between-study variability? Environ Health Perspect. 2000 Feb;108(2):109–117. doi: 10.1289/ehp.00108109. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Mar T. F., Norris G. A., Koenig J. Q., Larson T. V. Associations between air pollution and mortality in Phoenix, 1995-1997. Environ Health Perspect. 2000 Apr;108(4):347–353. doi: 10.1289/ehp.00108347. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Monn C., Becker S. Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air. Toxicol Appl Pharmacol. 1999 Mar 15;155(3):245–252. doi: 10.1006/taap.1998.8591. [DOI] [PubMed] [Google Scholar]
  14. Nel A. E., Diaz-Sanchez D., Li N. The role of particulate pollutants in pulmonary inflammation and asthma: evidence for the involvement of organic chemicals and oxidative stress. Curr Opin Pulm Med. 2001 Jan;7(1):20–26. doi: 10.1097/00063198-200101000-00004. [DOI] [PubMed] [Google Scholar]
  15. Pozzi Roberta, De Berardis Barbara, Paoletti Luigi, Guastadisegni Cecilia. Inflammatory mediators induced by coarse (PM2.5-10) and fine (PM2.5) urban air particles in RAW 264.7 cells. Toxicology. 2003 Feb 1;183(1-3):243–254. doi: 10.1016/s0300-483x(02)00545-0. [DOI] [PubMed] [Google Scholar]
  16. Schwartz D. A. Does inhalation of endotoxin cause asthma? Am J Respir Crit Care Med. 2001 Feb;163(2):305–306. doi: 10.1164/ajrccm.163.2.ed2000a. [DOI] [PubMed] [Google Scholar]
  17. Schwartz J., Norris G., Larson T., Sheppard L., Claiborne C., Koenig J. Episodes of high coarse particle concentrations are not associated with increased mortality. Environ Health Perspect. 1999 May;107(5):339–342. doi: 10.1289/ehp.99107339. [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Vincent R., Kumarathasan P., Goegan P., Bjarnason S. G., Guénette J., Bérubé D., Adamson I. Y., Desjardins S., Burnett R. T., Miller F. J. Inhalation toxicology of urban ambient particulate matter: acute cardiovascular effects in rats. Res Rep Health Eff Inst. 2001 Oct;(104):5–62. [PubMed] [Google Scholar]

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