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World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.

Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass...

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Autores principales: Gavett, Stephen H, Haykal-Coates, Najwa, Highfill, Jerry W, Ledbetter, Allen D, Chen, Lung Chi, Cohen, Mitchell D, Harkema, Jack R, Wagner, James G, Costa, Daniel L
Formato: Texto
Lenguaje:English
Publicado: 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241535/
https://www.ncbi.nlm.nih.gov/pubmed/12782502
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author Gavett, Stephen H
Haykal-Coates, Najwa
Highfill, Jerry W
Ledbetter, Allen D
Chen, Lung Chi
Cohen, Mitchell D
Harkema, Jack R
Wagner, James G
Costa, Daniel L
author_facet Gavett, Stephen H
Haykal-Coates, Najwa
Highfill, Jerry W
Ledbetter, Allen D
Chen, Lung Chi
Cohen, Mitchell D
Harkema, Jack R
Wagner, James G
Costa, Daniel L
author_sort Gavett, Stephen H
collection PubMed
description Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 microm (PM2.5)] has detrimental respiratory effects in mice to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM2.5 were derived from settled dust collected at several locations around Ground Zero on 12 and 13 September 2001. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 microg). This response was not as great as that caused by 100 microg PM2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 that would cause comparable doses in people are high (approximately 425 microg/m3 for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM2.5.
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spelling pubmed-12415352005-11-08 World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice. Gavett, Stephen H Haykal-Coates, Najwa Highfill, Jerry W Ledbetter, Allen D Chen, Lung Chi Cohen, Mitchell D Harkema, Jack R Wagner, James G Costa, Daniel L Environ Health Perspect Research Article Pollutants originating from the destruction of the World Trade Center (WTC) in New York City on 11 September 2001 have been reported to cause adverse respiratory responses in rescue workers and nearby residents. We examined whether WTC-derived fine particulate matter [particulate matter with a mass median aerodynamic diameter < 2.5 microm (PM2.5)] has detrimental respiratory effects in mice to contribute to the risk assessment of WTC-derived pollutants. Samples of WTC PM2.5 were derived from settled dust collected at several locations around Ground Zero on 12 and 13 September 2001. Aspirated samples of WTC PM2.5 induced mild to moderate degrees of pulmonary inflammation 1 day after exposure but only at a relatively high dose (100 microg). This response was not as great as that caused by 100 microg PM2.5 derived from residual oil fly ash (ROFA) or Washington, DC, ambient air PM [National Institute of Standards and Technology, Standard Reference Material (SRM) 1649a]. However, this same dose of WTC PM2.5 caused airway hyperresponsiveness to methacholine aerosol comparable to that from SRM 1649a and to a greater degree than that from ROFA. Mice exposed to lower doses by aspiration or inhalation exposure did not develop significant inflammation or hyperresponsiveness. These results show that exposure to high levels of WTC PM2.5 can promote mechanisms of airflow obstruction in mice. Airborne concentrations of WTC PM2.5 that would cause comparable doses in people are high (approximately 425 microg/m3 for 8 hr) but conceivable in the aftermath of the collapse of the towers when rescue and salvage efforts were in effect. We conclude that a high-level exposure to WTC PM2.5 could cause pulmonary inflammation and airway hyperresponsiveness in people. The effects of chronic exposures to lower levels of WTC PM2.5, the persistence of any respiratory effects, and the effects of coarser WTC PM are unknown and were not examined in these studies. Degree of exposure and respiratory protection, individual differences in sensitivity to WTC PM2.5, and species differences in responses must be considered in assessing the risks of exposure to WTC PM2.5. 2003-06 /pmc/articles/PMC1241535/ /pubmed/12782502 Text en
spellingShingle Research Article
Gavett, Stephen H
Haykal-Coates, Najwa
Highfill, Jerry W
Ledbetter, Allen D
Chen, Lung Chi
Cohen, Mitchell D
Harkema, Jack R
Wagner, James G
Costa, Daniel L
World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title_full World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title_fullStr World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title_full_unstemmed World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title_short World Trade Center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
title_sort world trade center fine particulate matter causes respiratory tract hyperresponsiveness in mice.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241535/
https://www.ncbi.nlm.nih.gov/pubmed/12782502
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