Effects of inhalable particulate matter on blood coagulation

M. Bonzini, A. Tripodi, A. Artoni, L. Tarantini, B. Marinelli, P. A. Bertazzi, P. Apostoli, A. Baccarelli

Research output: Contribution to journalArticle

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Abstract

Background: Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. Objectives: To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. Methods: We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, D-dimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of <1 μm (PM1) and coarse PM (PM10 - PM1). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Student's t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM1 and coarse PM exposure with parameter levels. Results: None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (β[PM1] = -0.33 s, P = 0.08; β[PMcoarse] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (β[PM1] = + 99 nm min, P = 0.02; β[PMcoarse] = + 66 nm min, P = 0.05), t-PA (β[PM1] = + 0.72 ng mL-1, P = 0.01; β[PMcoarse] = + 0.88 ng mL-1, P = 0.04), and CRP (β[PM1] = + 0.59 mg L-1, P = 0.03; β[PMcoarse] = + 0.48 mg L-1, P = 0.01). Conclusions: PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.

Original languageEnglish
Pages (from-to)662-668
Number of pages7
JournalJournal of Thrombosis and Haemostasis
Volume8
Issue number4
DOIs
Publication statusPublished - Apr 2010

Fingerprint

Particulate Matter
Blood Coagulation
Prothrombin Time
Thrombin
Thrombomodulin
Thrombophilia
C-Reactive Protein
Dilatation and Curettage
Partial Thromboplastin Time
Plasminogen Activators
Steel
Tissue Plasminogen Activator
Inhalation
Pneumonia
Thrombosis
Cardiovascular Diseases
Students
Inflammation
Antigens

Keywords

  • Coagulation
  • Endogenous thrombin potential
  • Environmental risk factors
  • Occupational health
  • Particulate matter

ASJC Scopus subject areas

  • Hematology

Cite this

Effects of inhalable particulate matter on blood coagulation. / Bonzini, M.; Tripodi, A.; Artoni, A.; Tarantini, L.; Marinelli, B.; Bertazzi, P. A.; Apostoli, P.; Baccarelli, A.

In: Journal of Thrombosis and Haemostasis, Vol. 8, No. 4, 04.2010, p. 662-668.

Research output: Contribution to journalArticle

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abstract = "Background: Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. Objectives: To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. Methods: We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, D-dimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of <1 μm (PM1) and coarse PM (PM10 - PM1). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Student's t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM1 and coarse PM exposure with parameter levels. Results: None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (β[PM1] = -0.33 s, P = 0.08; β[PMcoarse] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (β[PM1] = + 99 nm min, P = 0.02; β[PMcoarse] = + 66 nm min, P = 0.05), t-PA (β[PM1] = + 0.72 ng mL-1, P = 0.01; β[PMcoarse] = + 0.88 ng mL-1, P = 0.04), and CRP (β[PM1] = + 0.59 mg L-1, P = 0.03; β[PMcoarse] = + 0.48 mg L-1, P = 0.01). Conclusions: PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.",
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T1 - Effects of inhalable particulate matter on blood coagulation

AU - Bonzini, M.

AU - Tripodi, A.

AU - Artoni, A.

AU - Tarantini, L.

AU - Marinelli, B.

AU - Bertazzi, P. A.

AU - Apostoli, P.

AU - Baccarelli, A.

PY - 2010/4

Y1 - 2010/4

N2 - Background: Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. Objectives: To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. Methods: We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, D-dimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of <1 μm (PM1) and coarse PM (PM10 - PM1). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Student's t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM1 and coarse PM exposure with parameter levels. Results: None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (β[PM1] = -0.33 s, P = 0.08; β[PMcoarse] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (β[PM1] = + 99 nm min, P = 0.02; β[PMcoarse] = + 66 nm min, P = 0.05), t-PA (β[PM1] = + 0.72 ng mL-1, P = 0.01; β[PMcoarse] = + 0.88 ng mL-1, P = 0.04), and CRP (β[PM1] = + 0.59 mg L-1, P = 0.03; β[PMcoarse] = + 0.48 mg L-1, P = 0.01). Conclusions: PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.

AB - Background: Particulate matter (PM) exposure has been linked to increased risk of cardiovascular disease, possibly resulting from hypercoagulability and thrombosis. Lung and systemic inflammation resulting from PM inhalation may activate blood coagulation, but mechanisms for PM-related hypercoagulability are still largely unknown. Objectives: To identify coagulation mechanisms activated by PM in a population with well-characterized exposure. Methods: We measured prothrombin time (PT), activated partial thromboplastin time, endogenous thrombin potentials (ETPs) with/without exogenous triggers and with/without soluble thrombomodulin, tissue-type plasminogen activator (t-PA) antigen, D-dimer and C-reactive protein (CRP) in 37 workers in a steel production plant with well-characterized exposure to PM with aerodynamic diameter of <1 μm (PM1) and coarse PM (PM10 - PM1). Blood samples were collected from each subject on the first (baseline) and last (postexposure) day of a 4-day work week. We analyzed differences between baseline and postexposure levels using a paired Student's t-test. We fitted multivariate mixed-regression models to estimate the associations of interquartile range PM1 and coarse PM exposure with parameter levels. Results: None of the parameters showed any significant changes from baseline in postexposure samples. However, exposure levels were associated with shorter PT (β[PM1] = -0.33 s, P = 0.08; β[PMcoarse] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (β[PM1] = + 99 nm min, P = 0.02; β[PMcoarse] = + 66 nm min, P = 0.05), t-PA (β[PM1] = + 0.72 ng mL-1, P = 0.01; β[PMcoarse] = + 0.88 ng mL-1, P = 0.04), and CRP (β[PM1] = + 0.59 mg L-1, P = 0.03; β[PMcoarse] = + 0.48 mg L-1, P = 0.01). Conclusions: PM exposure did not show any short-term effect within the week of the study. The association of PM exposure with PT, ETP and CRP provides some evidence of long-term effects on inflammation and coagulation.

KW - Coagulation

KW - Endogenous thrombin potential

KW - Environmental risk factors

KW - Occupational health

KW - Particulate matter

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