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Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.
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MedLine Citation:
PMID:  12896848     Owner:  NLM     Status:  MEDLINE    
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.
Alvaro R Osornio-Vargas; James C Bonner; Ernesto Alfaro-Moreno; Leticia Martínez; Claudia García-Cuellar; Sergio Ponce-de-León Rosales; Javier Miranda; Irma Rosas
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Environmental health perspectives     Volume:  111     ISSN:  0091-6765     ISO Abbreviation:  Environ. Health Perspect.     Publication Date:  2003 Aug 
Date Detail:
Created Date:  2003-08-04     Completed Date:  2003-09-16     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0330411     Medline TA:  Environ Health Perspect     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1289-93     Citation Subset:  IM    
Instituto Nacional de Cancerología, Mexico City, México.
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MeSH Terms
Air Pollutants / toxicity*
Apoptosis / drug effects
Cell Line
Cell Survival / drug effects*
Inflammation / chemically induced*
Inflammation Mediators / metabolism
Interleukin-6 / biosynthesis
Particle Size
Tumor Necrosis Factor-alpha / biosynthesis
Reg. No./Substance:
0/Air Pollutants; 0/Inflammation Mediators; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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Journal Information
Journal ID (nlm-ta): Environ Health Perspect
ISSN: 0091-6765
Article Information
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Print publication date: Month: 8 Year: 2003
Volume: 111 Issue: 10
First Page: 1289 Last Page: 1293
ID: 1241608
PubMed Id: 12896848

Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition.
Alvaro R Osornio-Vargas
James C Bonner
Ernesto Alfaro-Moreno
Leticia Mart?nez
Claudia Garc?a-Cuellar
Sergio Ponce-de-Le?n Rosales
Javier Miranda
Irma Rosas
Instituto Nacional de Cancerolog?a, Mexico City, M?xico.

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