Effects of inhalable particulate matter on blood coagulation.
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.


OBJECTIVE
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 mum (PM(1)) and coarse PM (PM(10) - PM(1)). 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 PM(1) 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 (beta[PM(1)] = -0.33 s, P = 0.08; beta[PM(coarse)] = - 0.33 s, P = 0.01), and higher ETP without exogenous triggers and with thrombomodulin (beta[PM(1)] = + 99 nm min, P = 0.02; beta[PM(coarse)] = + 66 nm min, P = 0.05), t-PA (beta[PM(1)] = + 0.72 ng mL(-1), P = 0.01; beta[PM(coarse)] = + 0.88 ng mL(-1), P = 0.04), and CRP (beta[PM(1)] = + 0.59 mg L(-1), P = 0.03; beta[PM(coarse)] = + 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.
Bonzini
M
M
Department of Clinical and Biological Sciences, University of Insubria, Varese, Italy. matteo.bonzini@uninsubria.it
Tripodi
A
A
Artoni
A
A
Tarantini
L
L
Marinelli
B
B
Bertazzi
P A
PA
Apostoli
P
P
Baccarelli
A
A
D000328:Adult; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects*; D002097:C-Reactive Protein / Q000378:metabolism; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000139:chemically induced*; D018836:Inflammation Mediators / Q000097:blood; D019570:Inhalation Exposure; D007558:Italy; D008297:Male; D008669:Metallurgy; D008875:Middle Aged; D009784:Occupational Diseases / Q000097:blood / Q000139:chemically induced*; D016273:Occupational Exposure; D010314:Partial Thromboplastin Time; D010316:Particle Size; D052638:Particulate Matter / Q000009:adverse effects*; D011517:Prothrombin Time; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D013232:Steel / Q000009:adverse effects*; D013917:Thrombin / Q000378:metabolism; D019851:Thrombophilia / Q000097:blood / Q000139:chemically induced*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D052638:Particulate Matter; C036309:fibrin fragment D; D013232:Steel; D002097:C-Reactive Protein; D013917:Thrombin; D010959:Tissue Plasminogen Activator