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The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation

BACKGROUND: In the year 2000 Corus closed its steel plant operations in Redcar, NE of England temporarily for refurbishment of its blast furnace. This study investigates the impact of the closure on the chemical composition and biological activity of PM(10 )collected in the vicinity of the steel pla...

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Autores principales: Hutchison, Gary R, Brown, David M, Hibbs, Leon R, Heal, Mathew R, Donaldson, Ken, Maynard, Robert L, Monaghan, Michelle, Nicholl, Andy, Stone, Vicki
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156955/
https://www.ncbi.nlm.nih.gov/pubmed/15904485
http://dx.doi.org/10.1186/1465-9921-6-43
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author Hutchison, Gary R
Brown, David M
Hibbs, Leon R
Heal, Mathew R
Donaldson, Ken
Maynard, Robert L
Monaghan, Michelle
Nicholl, Andy
Stone, Vicki
author_facet Hutchison, Gary R
Brown, David M
Hibbs, Leon R
Heal, Mathew R
Donaldson, Ken
Maynard, Robert L
Monaghan, Michelle
Nicholl, Andy
Stone, Vicki
author_sort Hutchison, Gary R
collection PubMed
description BACKGROUND: In the year 2000 Corus closed its steel plant operations in Redcar, NE of England temporarily for refurbishment of its blast furnace. This study investigates the impact of the closure on the chemical composition and biological activity of PM(10 )collected in the vicinity of the steel plant. METHODS: The metal content of PM(10 )samples collected before during and after the closure was measured by ICP-MS in order to ascertain whether there was any significant alteration in PM(10 )composition during the steel plant closure. Biological activity was assessed by instillation of 24 hr PM(10 )samples into male Wistar rats for 18 hr (n = 6). Inflammation was identified by the cellular and biochemical profile of the bronchoalveolar lavage fluid. Metal chelation of PM(10 )samples was conducted using Chelex beads prior to treatment of macrophage cell line, J774, in vitro and assessment of pro-inflammatory cytokine expression. RESULTS: The total metal content of PM(10 )collected before and during the closure period were similar, but on reopening of the steel plant there was a significant 3-fold increase (p < 0.05) compared with the closure and pre-closure samples. Wind direction prior to the closure was predominantly from the north, compared to south westerly during the closure and re-opened periods. Of metals analysed, iron was most abundant in the total and acid extract, while zinc was the most prevalent metal in the water-soluble fraction. Elevated markers of inflammation included a significant increase (p < 0.01) in neutrophil cell numbers in the bronchoalveolar lavage of rats instilled with PM(10 )collected during the reopened period, as well as significant increases in albumin (p < 0.05). Extracts of PM(10 )from the pre-closure and closure periods did not induce any significant alterations in inflammation or lung damage. The soluble and insoluble extractable PM(10 )components washed from the reopened period both induced a significant increase in neutrophil cell number (p < 0.05) when compared to the control, and these increases when added together approximately equalled the inflammation induced by the whole sample. PM(10 )from the re-opened period stimulated J774 macrophages to generate TNF-α protein and this was significantly prevented by chelating the metal content of the PM(10 )prior to addition to the cells. CONCLUSION: PM(10)-induced inflammation in the rat lung was related to the concentration of metals in the PM(10 )samples tested, and activity was found in both the soluble and insoluble fractions of the particulate pollutant.
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spelling pubmed-11569552005-06-22 The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation Hutchison, Gary R Brown, David M Hibbs, Leon R Heal, Mathew R Donaldson, Ken Maynard, Robert L Monaghan, Michelle Nicholl, Andy Stone, Vicki Respir Res Research BACKGROUND: In the year 2000 Corus closed its steel plant operations in Redcar, NE of England temporarily for refurbishment of its blast furnace. This study investigates the impact of the closure on the chemical composition and biological activity of PM(10 )collected in the vicinity of the steel plant. METHODS: The metal content of PM(10 )samples collected before during and after the closure was measured by ICP-MS in order to ascertain whether there was any significant alteration in PM(10 )composition during the steel plant closure. Biological activity was assessed by instillation of 24 hr PM(10 )samples into male Wistar rats for 18 hr (n = 6). Inflammation was identified by the cellular and biochemical profile of the bronchoalveolar lavage fluid. Metal chelation of PM(10 )samples was conducted using Chelex beads prior to treatment of macrophage cell line, J774, in vitro and assessment of pro-inflammatory cytokine expression. RESULTS: The total metal content of PM(10 )collected before and during the closure period were similar, but on reopening of the steel plant there was a significant 3-fold increase (p < 0.05) compared with the closure and pre-closure samples. Wind direction prior to the closure was predominantly from the north, compared to south westerly during the closure and re-opened periods. Of metals analysed, iron was most abundant in the total and acid extract, while zinc was the most prevalent metal in the water-soluble fraction. Elevated markers of inflammation included a significant increase (p < 0.01) in neutrophil cell numbers in the bronchoalveolar lavage of rats instilled with PM(10 )collected during the reopened period, as well as significant increases in albumin (p < 0.05). Extracts of PM(10 )from the pre-closure and closure periods did not induce any significant alterations in inflammation or lung damage. The soluble and insoluble extractable PM(10 )components washed from the reopened period both induced a significant increase in neutrophil cell number (p < 0.05) when compared to the control, and these increases when added together approximately equalled the inflammation induced by the whole sample. PM(10 )from the re-opened period stimulated J774 macrophages to generate TNF-α protein and this was significantly prevented by chelating the metal content of the PM(10 )prior to addition to the cells. CONCLUSION: PM(10)-induced inflammation in the rat lung was related to the concentration of metals in the PM(10 )samples tested, and activity was found in both the soluble and insoluble fractions of the particulate pollutant. BioMed Central 2005 2005-05-18 /pmc/articles/PMC1156955/ /pubmed/15904485 http://dx.doi.org/10.1186/1465-9921-6-43 Text en Copyright © 2005 Hutchison et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Hutchison, Gary R
Brown, David M
Hibbs, Leon R
Heal, Mathew R
Donaldson, Ken
Maynard, Robert L
Monaghan, Michelle
Nicholl, Andy
Stone, Vicki
The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title_full The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title_fullStr The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title_full_unstemmed The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title_short The effect of refurbishing a UK steel plant on PM(10 )metal composition and ability to induce inflammation
title_sort effect of refurbishing a uk steel plant on pm(10 )metal composition and ability to induce inflammation
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1156955/
https://www.ncbi.nlm.nih.gov/pubmed/15904485
http://dx.doi.org/10.1186/1465-9921-6-43
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