Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.

P. S. Gilmour, A. Ziesenis, Elspeth Rona Morrison, Mark Adrian Vickers, E. M. Drost, Isobel Ford, E. Karg, C. Mossa, A. Schroeppel, G. A. Ferron, J. Heyder, Michael Greaves, W. MacNee, K. Donaldson

Research output: Contribution to journalArticle

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Abstract

While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h, The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 It postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB. (C) 2003 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)35-44
Number of pages9
JournalToxicology and Applied Pharmacology
Volume195
DOIs
Publication statusPublished - 2004

Keywords

  • cardiovascular
  • PM10
  • ultrafine
  • particles
  • PARTICULATE AIR-POLLUTION
  • OXIDATIVE STRESS
  • EPITHELIAL-CELLS
  • LUNG-FUNCTION
  • CARDIOVASCULAR-DISEASE
  • RESPIRATORY HEALTH
  • TRANSITION-METALS
  • SURFACE-AREA
  • URBAN AIR
  • IN-VITRO

Cite this

Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles. / Gilmour, P. S.; Ziesenis, A.; Morrison, Elspeth Rona; Vickers, Mark Adrian; Drost, E. M.; Ford, Isobel; Karg, E.; Mossa, C.; Schroeppel, A.; Ferron, G. A.; Heyder, J.; Greaves, Michael; MacNee, W.; Donaldson, K.

In: Toxicology and Applied Pharmacology, Vol. 195, 2004, p. 35-44.

Research output: Contribution to journalArticle

Gilmour, PS, Ziesenis, A, Morrison, ER, Vickers, MA, Drost, EM, Ford, I, Karg, E, Mossa, C, Schroeppel, A, Ferron, GA, Heyder, J, Greaves, M, MacNee, W & Donaldson, K 2004, 'Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.' Toxicology and Applied Pharmacology, vol. 195, pp. 35-44. https://doi.org/10.1016/j.taap.2003.10.003
Gilmour, P. S. ; Ziesenis, A. ; Morrison, Elspeth Rona ; Vickers, Mark Adrian ; Drost, E. M. ; Ford, Isobel ; Karg, E. ; Mossa, C. ; Schroeppel, A. ; Ferron, G. A. ; Heyder, J. ; Greaves, Michael ; MacNee, W. ; Donaldson, K. / Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles. In: Toxicology and Applied Pharmacology. 2004 ; Vol. 195. pp. 35-44.
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T1 - Pulmonary and systemic effects of short-term inhalation exposure to ultrafine carbon black particles.

AU - Gilmour, P. S.

AU - Ziesenis, A.

AU - Morrison, Elspeth Rona

AU - Vickers, Mark Adrian

AU - Drost, E. M.

AU - Ford, Isobel

AU - Karg, E.

AU - Mossa, C.

AU - Schroeppel, A.

AU - Ferron, G. A.

AU - Heyder, J.

AU - Greaves, Michael

AU - MacNee, W.

AU - Donaldson, K.

PY - 2004

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N2 - While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h, The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 It postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB. (C) 2003 Elsevier Inc. All rights reserved.

AB - While environmental particles are associated with mortality and morbidity related to pulmonary and cardiovascular (CV) disease, the mechanisms involved in CV health effects are not known. Changes in systemic clotting factors have been associated with pulmonary inflammation. We hypothesized that inhaled ultrafine particles result in an inflammatory response which may stimulate systemic clotting factor release. Adult male Wistar rats were exposed to either fine or ultrafine carbon black (CB) for 7 h, The attained total suspended particle concentrations were 1.66 mg/m(3) for ultrafine CB and 1.40 mg/m(3) for fine CB. Particle concentration of ultrafine particles was more than 10 times greater than that of fine particles and the count median aerodynamic diameter averaged 114 nm for the ultrafine and 268 nm for the fine carbon particles. Data were collected immediately, 16 and 48 h following exposure. Only ultrafine CB caused an increase in total bronchoalveolar lavage (BAL) leukocytes, whereas both fine (2-fold) and ultrafine (4-fold) carbon particles caused an increase in BAL neutrophils at 16 It postexposure. Exposure to the ultrafine, but not fine, carbon was also associated with significant increases in the total numbers of blood leukocytes. Plasma fibrinogen, factor VII and von Willebrand factor (vWF) were unaffected by particle treatments as was plasma Trolox equivalent antioxidant status (TEAC). Macrophage inflammatory protein-2 mRNA was significantly increased in BAL cells 48 h following exposure to ultrafine CB. The data show that there is a small but consistent significant proinflammatory effect of this exposure to ultrafine particles that is greater than the effect of the same exposure to fine CB. (C) 2003 Elsevier Inc. All rights reserved.

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KW - PM10

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KW - OXIDATIVE STRESS

KW - EPITHELIAL-CELLS

KW - LUNG-FUNCTION

KW - CARDIOVASCULAR-DISEASE

KW - RESPIRATORY HEALTH

KW - TRANSITION-METALS

KW - SURFACE-AREA

KW - URBAN AIR

KW - IN-VITRO

U2 - 10.1016/j.taap.2003.10.003

DO - 10.1016/j.taap.2003.10.003

M3 - Article

VL - 195

SP - 35

EP - 44

JO - Toxicology and Applied Pharmacology

JF - Toxicology and Applied Pharmacology

SN - 0041-008X

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