A brief review of the biology of megakaryocytes and platelets and their role in thrombosis associated with particulate air pollution

Abstract

Air pollution is a worldwide public health issue and it is associated with millions of premature deaths due to cancer, thrombosis, and pulmonary and cardiovascular diseases. Thrombosis is the excessive clotting that blocks a blood vessel, and its etiology is multifactorial. In recent years, growing evidence has linked air pollution, especially particulate matter (PM) and metals, to the development of thrombosis. PM and metals induce lung and systemic inflammation and oxidative stress that are frequent mechanisms in thrombosis. Platelets are important effectors of physiological hemostasis and pathological thrombosis. They are responsible for the formation of the initial plug and are important in the cellular model of coagulation. Therefore, any changes in their morphology or function or an increase in activation could be extremely relevant in thrombosis. Megakaryocytes (MKs) in the bone marrow and in the lungs are the precursor cells of platelets, and the latter is the first organ injured by air pollution. There is substantial evidence of the effect that PM and metals have on platelets, but there is almost no research about the effect of PM and metals on MKs. It is very likely that the alterations produced by air pollution originate in these cells. In this article, we review the biology of MKs and platelets and their role in particulate air pollution-related thrombosis to emphasize the need for further research in this field.

Interactions of platelets with obesity in relation to lung cancer risk in the UK Biobank cohort

“…We were also unable to examine thrombopoiesis and platelet maturity. Our project did not have access to the information for air pollution available in UK Biobank, as examining this was beyond the scope of our project but merits investigation in future studies because air pollution is associated with platelet activation [ 65 ], as well as with higher risk of lung cancer [ 66 ]. Some residual confounding from smoking is possible for the positive association with PLT, as smoking was the most influential covariate.…”