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Published on: December 10, 2021
Short-term exposure to particulate matter induces arterial but not venous thrombosis in healthy mice
J Emmerechts1, E Alfaro-Moreno, B M Vanaudenaerde
1Center for Molecular and Vascular Biology, Katholieke Universiteit Leuven, Leuven, Belgium.
Background:
Epidemiological findings suggest an association between exposure to particulate matter (PM) and venous thrombo-embolism.
Objectives:
To investigate arterial vs. venous thrombosis, inflammation and coagulation in mice, (sub)acutely exposed to two types of PM.
Methods:
Various doses (25, 100 and 200 μg per animal) of urban particulate matter (UPM) or diesel exhaust particles (DEP) were intratracheally (i.t.) instilled in C57Bl6/n mice and several endpoints measured at 4, 10 and 24 h. Mice were also repeatedly exposed to 100 μg per animal on three consecutive days with endpoints measured 24 h after the last instillation.
Results:
Exposure to 200 μg per mouse UPM enhanced arterial thrombosis, but neither UPM nor DEP significantly enhanced venous thrombosis. Both types of PM induced dose-dependent increases in broncho-alveolar lavage fluid (BALF) total cell numbers (mainly neutrophils) and cytokines (IL-6, KC, MCP-1, RANTES, MIP-1α), with peaks at 4 h and overall higher values for UPM than for DEP. Systemic inflammation was limited to increased serum IL-6 levels, 4 h after UPM. Both types of PM induced similar and dose-dependent but modest increases in factor (F)VII, FVIII and fibrinogen. Three repeated instillations did not or only modestly enhance the proinflammatory and procoagulant status.
Conclusions:
Compared with DEP, UPM induced more pronounced pulmonary inflammation, but both particle types triggered similar and mild short-term systemic effects. Hence, acute exposure to PM triggers activation of primary hemostasis in the mouse, but no substantial secondary hemostasis activation, resulting in arterial but not venous thrombogenicity.
Insights
Exposure to particulate matter (PM) can increase arterial thrombosis risk. While both urban (UPM) and diesel exhaust particles (DEP) cause lung inflammation, they only mildly affect blood clotting, leading to arterial but not venous clot formation.
Area of Science:
- Environmental Health
- Toxicology
- Cardiovascular Research
Background:
- Epidemiological studies link particulate matter (PM) exposure to venous thromboembolism.
- Understanding PM's impact on thrombosis is crucial for public health.
Purpose of the Study:
- To investigate the effects of urban particulate matter (UPM) and diesel exhaust particles (DEP) on arterial and venous thrombosis.
- To assess inflammation and coagulation changes in mice following acute and sub-acute PM exposure.
Main Methods:
- Mice were intratracheally instilled with UPM or DEP at various doses.
- Endpoints including thrombosis, inflammation markers, and coagulation factors were measured at different time points.
- Repeated exposure protocols were also employed.
Main Results:
- UPM exposure (200 μg) enhanced arterial thrombosis; neither UPM nor DEP significantly affected venous thrombosis.
- Both PM types induced dose-dependent pulmonary inflammation (neutrophils, cytokines) and mild systemic IL-6 increase.
- Modest, dose-dependent increases in coagulation factors (FVII, FVIII, fibrinogen) were observed.
Conclusions:
- UPM caused more pronounced pulmonary inflammation than DEP, but both induced similar mild short-term systemic effects.
- Acute PM exposure activates primary hemostasis, leading to arterial thrombogenicity.
- No substantial secondary hemostasis activation was observed, indicating limited venous thrombotic risk.
