Pulmonary exposure to carbon black nanoparticles and vascular effects

Lise K Vesterdal; Janne K Folkmann; Nicklas R Jacobsen; Majid Sheykhzade; Håkan Wallin; Steffen Loft; Peter Møller

doi:10.1186/1743-8977-7-33

Pulmonary exposure to carbon black nanoparticles and vascular effects

Lise K Vesterdal, Janne K Folkmann, Nicklas R Jacobsen, Majid Sheykhzade, Håkan Wallin, Steffen Loft, Peter Møller

71 Citations (Scopus)

Abstract

Background: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Methods: We exposed young and aged apolipoprotein E knockout mice (apoE^-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.Results: Young apoE^-/-mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged apoE^-/-mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged apoE^-/-mice. The expression of MCP-1 mRNA was increased in the lungs of young apoE^-/-mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged apoE^-/-mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.Conclusion: Exposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.

Original language	English
Journal	Particle and Fibre Toxicology
Volume	7
Pages (from-to)	33
ISSN	1743-8977
DOIs	https://doi.org/10.1186/1743-8977-7-33
Publication status	Published - 5 Nov 2010

Keywords

Administration, Inhalation
Aging
Animals
Apolipoproteins E
Bronchoalveolar Lavage Fluid
Chemokine CCL2
Heme Oxygenase-1
Intercellular Adhesion Molecule-1
Lung
Mice
Mice, Knockout
Muscle Contraction
Muscle, Smooth, Vascular
Nanoparticles
Oxidative Stress
Plaque, Atherosclerotic
Pneumonia
Soot
Time Factors
Tyrosine
Vascular Cell Adhesion Molecule-1

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/1743-8977-7-33

Cite this

@article{d8b9173e675246ceafb2ca41c8ef050a,

title = "Pulmonary exposure to carbon black nanoparticles and vascular effects",

abstract = "Background: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Methods: We exposed young and aged apolipoprotein E knockout mice (apoE-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.Results: Young apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged apoE-/- mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged apoE-/- mice. The expression of MCP-1 mRNA was increased in the lungs of young apoE-/- mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.Conclusion: Exposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.",

keywords = "Administration, Inhalation, Aging, Animals, Apolipoproteins E, Bronchoalveolar Lavage Fluid, Chemokine CCL2, Heme Oxygenase-1, Intercellular Adhesion Molecule-1, Lung, Mice, Mice, Knockout, Muscle Contraction, Muscle, Smooth, Vascular, Nanoparticles, Oxidative Stress, Plaque, Atherosclerotic, Pneumonia, Soot, Time Factors, Tyrosine, Vascular Cell Adhesion Molecule-1",

author = "Vesterdal, {Lise K} and Folkmann, {Janne K} and Jacobsen, {Nicklas R} and Majid Sheykhzade and H{\aa}kan Wallin and Steffen Loft and Peter M{\o}ller",

year = "2010",

month = nov,

day = "5",

doi = "10.1186/1743-8977-7-33",

language = "English",

volume = "7",

pages = "33",

journal = "Particle and Fibre Toxicology",

issn = "1743-8977",

publisher = "BioMed Central",

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TY - JOUR

T1 - Pulmonary exposure to carbon black nanoparticles and vascular effects

AU - Vesterdal, Lise K

AU - Folkmann, Janne K

AU - Jacobsen, Nicklas R

AU - Sheykhzade, Majid

AU - Wallin, Håkan

AU - Loft, Steffen

AU - Møller, Peter

PY - 2010/11/5

Y1 - 2010/11/5

N2 - Background: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Methods: We exposed young and aged apolipoprotein E knockout mice (apoE-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.Results: Young apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged apoE-/- mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged apoE-/- mice. The expression of MCP-1 mRNA was increased in the lungs of young apoE-/- mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.Conclusion: Exposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.

AB - Background: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Methods: We exposed young and aged apolipoprotein E knockout mice (apoE-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.Results: Young apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged apoE-/- mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged apoE-/- mice. The expression of MCP-1 mRNA was increased in the lungs of young apoE-/- mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.Conclusion: Exposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.

KW - Administration, Inhalation

KW - Aging

KW - Animals

KW - Apolipoproteins E

KW - Bronchoalveolar Lavage Fluid

KW - Chemokine CCL2

KW - Heme Oxygenase-1

KW - Intercellular Adhesion Molecule-1

KW - Lung

KW - Mice

KW - Mice, Knockout

KW - Muscle Contraction

KW - Muscle, Smooth, Vascular

KW - Nanoparticles

KW - Oxidative Stress

KW - Plaque, Atherosclerotic

KW - Pneumonia

KW - Soot

KW - Time Factors

KW - Tyrosine

KW - Vascular Cell Adhesion Molecule-1

U2 - 10.1186/1743-8977-7-33

DO - 10.1186/1743-8977-7-33

M3 - Journal article

C2 - 21054825

SN - 1743-8977

VL - 7

SP - 33

JO - Particle and Fibre Toxicology

JF - Particle and Fibre Toxicology

ER -

Pulmonary exposure to carbon black nanoparticles and vascular effects

Abstract

Keywords

UN SDGs

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