Effects of inhalable particulate matter on blood coagulation


Matteo Bonzini, Department of Clinical and Biological Sciences, University of Insubria, Ospedale di Circolo, Viale Borri 57, 21100 Varese, Italy.
Tel.: +39 332393289; fax: +39 332278986.
E-mail: matteo.bonzini@uninsubria.it


See also Mannucci PM. Fine particulate: it matters. This issue, pp 659–61; Dales RE, Cakmak S, Vidal CB. Air pollution and hospitalization for venous thromboembolic disease in Chile. This issue, pp 669–74.

Summary. 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 nmin, 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.